Search PubMed⌕ Search

Biomedical subjects

H C Hopf

Publications and source records attributed to H C Hopf.

At least 37 records · Page 2Linked to original sources

Adaptive frequency decomposition of EEG with subsequent expert system analysis.

We present a hybrid system for automatic analysis of clinical routine EEG, comprising a spectral analysis and an expert system. EEG raw data are transformed into the time-frequency domain by the so-called adaptive frequency decomposition. The resulting frequency components are converted into pseudo-linguistic facts via fuzzification. Finally, an expert system applies symbolic rules formulated by the neurologist to evaluate the extracted EEG features. The system detects artefacts, describes alpha rhythm by frequency, amplitude, and stability and after artefact rejection detects pathologic slow activity. All results are displayed as linguistic terms, numerical values and maps of temporal extent, giving an overview about the clinical routine EEG.

Adolescent↗

Time course of lesion development in patients with acute brain stem infarction and correlation with NIHSS score.

BACKGROUND AND PURPOSE: diffusion weighted magnetic resonance imaging (MRI) is highly sensitive in detecting acute supratentorial cerebral ischemia and Diffusion Weighted Imaging (DWI) lesion size has been shown to correlate strongly with the neurologic deficit in middle cerebral artery territory stroke. However, data concerning infratentorial strokes are rare. We examined the size and evolution of acute brain stem ischemic lesions and their relationship to neurological outcome. METHODS: brain stem infarctions of 11 patients were analyzed. We performed DWI in all patients and in 7/11 patients within 24 h, T2W sequences within the first 2 weeks (10/11 patients) and follow-up MRI (MR2) within 3-9 months (median 4.8 months) later (12/12 patients). Lesion volumes were compared with early and follow-up neurologic deficit as determined by National Institutes of Health Stroke Scale (NIHSS) score. RESULTS: the relative infarct volumes--with MR2 lesion size set to 100%--decreased over the time (P<0.02) with a mean shrinking factor of 3.3 between DWI (MR0) and the follow-up MRT (P<0.02), and 1.6 between early T2W (MR1) and MR2 (P<0.04). The mean DWI volume size (MR0) was larger than the early T2W (P<0.02). Although neurological outcome was good in all patients (mean NIHSS score of 1.3 at follow-up), early NIHSS and follow-up NIHSS scores were strongly correlated (r=0.9, P<0.00). NIHSS score at follow-up was highly correlated with lesion size of DWI (MR0; r=0.71, P<0.04) and T2W of MR1 (r=0.86, P<0.001). CONCLUSIONS: in this study, we saw a shrinking of the brain stem infarct volume according to clinical improvement of patients. Great extension of restricted diffusion in the acute stage does not necessarily implicate a large resulting infarction or a bad clinical outcome.

Brain Stem Infarctions↗

A new method to investigate brain stem structural-functional correlations using digital post-processing MRI--reliability in ischemic internuclear ophthalmoplegia.

We investigated the reliability of a new digital post-processing magnetic resonance imaging (MRI) technique in ischemic brain stem lesions to identify relations of the lesion to anatomical brain stem structures. The target was a medial longitudinal fasciculus (MLF) lesion, which was evident from ipsilateral internuclear ophthalmoplegia (INO). Sixteen patients with acute unilateral INO and an isolated acute brain stem lesion in T2- and EPI-diffusion weighted MRI within 2 days after the onset of symptoms were studied. The MRI slice direction was parallel and perpendicular to a slice selection of a stereotactic anatomical atlas. The individual slices were normalized and projected in the digitalized atlas. The eye movement disorder was monitored by electro-oculography. In all patients with clinical or subclinical electro-oculographically documented INO and MRI proven brain stem infarction the lesion covered or at least partially overlapped the ipsilateral MLF at one or more atlas levels. We conclude that digital post-processing MRI with normalizing and projecting brain stem lesions in an anatomical atlas is a reliable method to demonstrate the anatomical structures involved by the lesion. Combined with electrophysiological brain stem testing, this method may be a useful tool to identify incompletely understood pathways mediating brain stem reflexes or the generators of evoked potentials.

Adult↗

The course of corticofacial projections in the human brainstem.

Transcranial magnetic stimulation was used to investigate the corticofacial projections in 53 patients with (n = 28) and without (n = 25) central facial paresis due to unifocal ischaemic lesions at different brainstem levels. Lesion topography documented by MRI studies was correlated with the electrophysiological findings. In the majority of patients the corticofacial fibres travel within the ventromedial base of the pons and cross the midline at the level of the facial nucleus. In some individuals, however, we found evidence that corticolingual fibres form an 'aberrant bundle' in a paralemniscal position at the dorsal edge of the pontine base. In other patients the corticofacial fibres loop down into the ventral part of the upper medulla, cross the midline and ascend in the dorsolateral medullary region ipsilaterally to the facial nucleus. The findings suggest that facial paresis due to a brainstem lesion may present as contralateral supranuclear facial paresis by a lesion of the cerebral peduncle, pontine base, the aberrant bundle and the ventral medulla. Supranuclear facial paresis ipsilateral to the lesion side may result from a lesion in the lateral medulla, and facial paresis of the supranuclear type may be imitated by a lesion of the peripheral facial nerve in the dorsolateral medulla with involvement of the lower pons.

Brain Stem↗

The masseter reflex: postprocessing methods and influence of age and gender. Normative values of the masseter reflex.

OBJECTIVES: Normative values of the masseter reflex are scarce. We studied the latencies, amplitudes and side differences of the masseter reflex in 105 healthy volunteers between the ages of 5 and 78 years. METHODS: Latencies were calculated as the mean of 10 single sweeps and, simultaneously, measured from the summation curve. Short-term reproducibility was determined in 33 volunteers by retesting the reflex after 1 week. RESULTS: There was a positive correlation between age and latencies and a negative correlation between age and amplitude. Maximal normal latencies were 8.3 ms for men and 7.9 ms for women in the age group below 50 years and 9.1 and 9.2 ms for the age group above 50 years. Latency differences between the right and left sides of >0.4 ms for subjects aged below 50 years and >0.5 ms for subjects aged above 50 years exceeded the 95% confidence interval. Amplitudes did not depend on gender. Calculated as a percentage of the side with higher amplitude, differences above one third could be accepted as abnormal. CONCLUSION: The masseter reflex appears to be a stable and robust clinical test, if age and gender differences are taken into account.

Adolescent↗

Lack of association between carotid artery volume blood flow and cardiac output.

OBJECTIVE: The correlation of cardiac output and cerebral perfusion is unclear. We tested this potential association by correlating cardiac output data obtained by echocardiography and cerebral blood flow data as determined by color M-mode measurements of carotid artery blood flow. METHODS: We studied 43 patients with a broad spectrum of cardiac performance by means of transthoracic echocardiography. In these patients, different cardiac indices such as stroke volume, ejection fraction, and heart minute volume were determined. The data were correlated with volumetric flow measurements (color M-mode duplex system) of the common carotid arteries bilaterally. RESULTS: Heart minute volume ranged from 1.632 to 9.836 mL/min (mean +/- SD, 4.652 +/- 1.621 mL/min); ejection fraction ranged from 18% to 76% (mean, 48% +/- 16%). The relative fraction of carotid volume flow compared with heart minute volume was 15% +/- 6%. There was no correlation between ejection fraction, stroke volume, or heart minute volume and absolute volume flow in the carotid arteries when being adjusted for age. There was a highly significant inverse correlation (r = -0.8; P < .0001) of the relative fraction of the carotid volume flow (carotid volume flow/heart minute volume [percent]) and the heart minute volume. CONCLUSION: Our data support the concept that cerebral blood flow is independent of cardiac output.

Cardiac Output↗

Mechanisms and predictors of chronic facial pain in lateral medullary infarction.

The purpose of this study was to identify clinical predictors and anatomical structures involved in patients with pain after dorsolateral medullary infarction. Eight out of 12 patients (67%) developed poststroke pain within 12 days to 24 months after infarction. The pain occurred in the ipsilateral face (6 patients) and/or the contralateral limbs and trunk (5 patients, 3 of whom also had facial pain). Ipsilateral facial pain was significantly correlated with lower medullary lesions, including those of the spinal trigeminal tract and/or nucleus, as documented by magnetic resonance imaging. The R2 blink reflex component was abnormal only in patients with facial pain. Likewise, pain and temperature sensation in the ipsilateral face was decreased in all patients with facial pain but not in patients without pain. Ipsilateral touch sensation in the face was also decreased in all patients with facial pain, but the lesions revealed on magnetic resonance imaging did not involve the principal sensory nucleus of the fifth cranial nerve, and the R1 blink reflex latencies were normal. Although facial pain was correlated with lesions of the spinal trigeminal tract and/or nucleus, none of the lesions involved the subnucleus caudalis, which contains most nociceptive neurons. These findings suggest that facial pain after medullary infarction is due to lesions of the lower spinal trigeminal tract (axons of primary afferent neurons), leading to deafferentation of spinal trigeminal nucleus neurons.

Aged↗

Masseter reflex latencies and amplitudes are not influenced by supratentorial and cerebellar lesions.

The aim of this study was to investigate possible influences of suprasegmental lesions on the masseter reflex. The masseter reflex was elicited in 54 patients with supratentorial (37 patients) or cerebellar (17 patients) lesions 3-11 days after the acute onset of clinical disease. Patients showing lesions within the pons and midbrain on thin-slice magnetic resonance imaging were excluded from evaluation. The testing procedure included an additional facilitating maneuver (opening and closing the jaw before tapping). Masseter reflex latencies, interside differences, and amplitudes were within the normal range in all patients. Latencies were not different with and without the facilitating maneuver. Amplitudes were significantly higher with the maneuver, but interside differences of amplitudes were unchanged. Masseter reflex abnormality can be taken as a reliable measure of direct involvement of the reflex arc.

Adult↗

Isolated superior oblique palsies with electrophysiologically documented brainstem lesions.

Over a 13.5-year period, we observed 10 patients with isolated superior oblique palsies in whom electrophysiological abnormalities indicated brainstem lesions. In 7 patients unilateral masseter reflex abnormalities were seen, and were located on the side of the superior oblique palsy in 2 patients and on the opposite side in 5 patients. Two patients had slowed gain of following eye movements to the side contralateral to the superior oblique palsy. Slowed adduction saccades in the eye contralateral to the superior oblique palsy were seen in 1 patient. Clinical improvement was frequently (in 7 of 10 patients) associated with improvement or normalization of electrophysiologic findings. Magnetic resonance imaging (MRI) was normal, showing no evidence of brainstem lesions in 6 patients. Unilateral superior oblique palsy may be the only clinical sign of a brainstem lesion. Although such a cause may be underdiagnosed if based on MRI-documented lesions only, it remains a rare condition.

Adult↗

EDSS correlated analysis of median nerve somatosensory evoked potentials in multiple sclerosis.

Median nerve somatosensory evoked potentials (SEP) were recorded in 30 patients with multiple sclerosis. The examined patients had an expanded disability status scale (EDSS) between 0 and 6. The primary cortical potential N20, the subcortical potentials P14, N13b, N13a and the peripheral potential P9 were recorded simultaneously. In 5 patients normal SEP were observed (group 1), and in 6 patients there were consecutive disturbances of the somatosensory pathway (group 3). In 19 patients subcortical potentials were abnormal or absent while the following potentials were normal or identified which pattern corresponds to amplification within CNS structures (group 2). The EDSS of groups 1 and 2 were similar and lower than the EDSS of group 3, which indicates that amplification mechanisms could represent a positive prognostic factor in SEP diagnosis of multiple sclerosis.

Adult↗

Assessment of brainstem function in Chiari II malformation utilizing brainstem auditory evoked potentials (BAEP), blink reflex and masseter reflex.

Brainstem dysfunction was evaluated in 67 patients with myelomeningocele and Chiari II malformation using brainstem auditory evoked potentials (BAEP), blink reflex (BR) and masseter reflex (MR). Signs and symptoms related to Chiari II malformation were observed in 18 patients while 49 patients had normal brainstem findings. BAEP and BR showed a higher sensitivity of brainstem involvement than MR (BAEP=1.0, BR=0.83, MR=0.50). BR, and in particular, MR were of higher accuracy (BR=0.52, MR=0.72) than BAEP (0.39) in separating patients with brainstem signs and symptoms related to Chiari II malformation. We feel that this is due to anatomic and physiologic peculiarities of the brainstem structures mediating BR and MR. Our results suggest that brainstem reflexes can support the decision of further treatment.

Adolescent↗

Scalp, basal epidural and intravascular far-field recordings after median nerve stimulation: evidence for a separate N18a potential.

Far-field somatosensory evoked potentials (SSEPs) after median nerve stimulation were recorded from scalp- (Fz), epidural- (ED) and intravascular electrodes (basilar artery [Bas]) to study the nature of the controversial N18a component of the widespread N18 potential. In healthy volunteers frequently an N18a potential was recorded at Fz. Simultaneous Fz and ED recordings at the pontomesencephalic junction as well as Bas-recordings at the caudal basilar artery showed N18a components identical in latency and shape. With intravascular recordings the shapes differed between the top of the basilar artery and the caudal artery recordings. These findings support the existence of a separate N18a potential. The generator of the N18a is likely to be localized within the upper brainstem.

Arteriovenous Malformations↗

Muscle fiber conduction velocity at different states of isotonic contraction.

Conduction velocity (CV), relative twitch force (RTF) and contraction time (CT) of single muscle fibers (SF) and small muscle fiber bundles (FB) were measured at different states of isotonic contraction with double impulse stimuli at varying interstimulus intervals (ISI) from 0 to 1000 ms in the biceps brachii muscle in vivo. During an isotonic contraction, muscle fibers conducted the action potential on average 0.18 m/s faster along the muscle fiber membrane than did relaxed muscle fibers. This difference was statistically significant (P < 0.001). There was a significant positive correlation between the degree of isotonic contraction and fiber bundle conduction velocity (FBCV) with a first peak at the maximum RTF at an ISI of 9 ms and a second peak at the maximum CT at an ISI of 100 ms.

Adult↗

[Indications for simultaneous origin of a German and American family with type II hereditary amyloid neuropathy].

The classification of familial amyloid neuropathies (FAP) is traditionally based on clinical and regional aspects. In the last 10 years more than 40 mutations of the transthyretin gene have been found to be responsible for different clinical forms of amyloidosis including familial FAP.FAP II is caused by a mutation on the codon 58 of the transthyretin gene. Only two american kindreds (the Maryland/German and the Ohio family) have previously been reported with FAP II starting in the 3rd or 4th decade by sensory disturbances of the hands typically as a carpal tunnel syndrome. We report on a german family with FAP II from the rhine river area south of Mainz. Four members with typical clinical symptoms showed the histidine 58 mutation like the american families with FAP II. Haplotype analysis showed that all of them were haplotype III like the american patients indicating that the american and german kindreds have a genetic linkage and common familial roots.

Adult↗